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3. Reduction of BMPR2 mRNA Expression in Peripheral Blood of Pulmonary Arterial Hypertension Patients: A Marker for Disease Severity?

Author

Theobald, Vivienne, Benjamin, Nicola, Seyfarth, Hans-Jürgen, Halank, Michael, Schneider, Marc A., Richtmann, Sarah, Hinderhofer, Katrin, Xanthouli, Panagiota, Egenlauf, Benjamin, Seeger, Rebekka, Hoeper, Marius M., Jonigk, Danny, Grünig, Ekkehard, Eichstaedt, Christina A., Theobald, Vivienne, Benjamin, Nicola, Seyfarth, Hans-Jürgen, Halank, Michael, Schneider, Marc A., Richtmann, Sarah, Hinderhofer, Katrin, Xanthouli, Panagiota, Egenlauf, Benjamin, Seeger, Rebekka, Hoeper, Marius M., Jonigk, Danny, Grünig, Ekkehard, and Eichstaedt, Christina A.

Abstract

Pulmonary arterial hypertension (PAH) can be caused by pathogenic variants in the gene bone morphogenetic protein receptor 2 (BMPR2). While BMPR2 protein expression levels are known to be reduced in the lung tissue of heritable PAH (HPAH) patients, a systematic study evaluating expression in more easily accessible blood samples and its clinical relevance is lacking. Thus, we analyzed the BMPR2 mRNA expression in idiopathic/HPAH patients and healthy controls in blood by quantitative polymerase chain reaction and protein expression by enzyme-linked immunosorbent assay. Clinical parameters included right heart catherization, echocardiography, six-minute walking test and laboratory tests. BMPR2 variant-carriers (n = 23) showed significantly lower BMPR2 mRNA expression in comparison to non-carriers (n = 56) and healthy controls (n = 30; p < 0.0001). No difference in BMPR2 protein expression was detected. Lower BMPR2 mRNA expression correlated significantly with greater systolic pulmonary artery pressure and pulmonary vascular resistance. Higher BMPR2 mRNA expression correlated with greater glomerular filtration rate, cardiac index and six-minute walking distance. We demonstrated the feasibility to assess BMPR2 expression in blood and, for the first time, that BMPR2 mRNA expression levels are significantly reduced in variant carriers and correlated with clinical parameters. Further studies may evaluate the usefulness of BMPR2 mRNA expression in blood as a new marker for disease severity.

Published
2022

4. Reduction of BMPR2 mRNA Expression in Peripheral Blood of Pulmonary Arterial Hypertension Patients: A Marker for Disease Severity?

Author

Theobald, Vivienne, primary, Benjamin, Nicola, additional, Seyfarth, Hans-Jürgen, additional, Halank, Michael, additional, Schneider, Marc A., additional, Richtmann, Sarah, additional, Hinderhofer, Katrin, additional, Xanthouli, Panagiota, additional, Egenlauf, Benjamin, additional, Seeger, Rebekka, additional, Hoeper, Marius M., additional, Jonigk, Danny, additional, Grünig, Ekkehard, additional, and Eichstaedt, Christina A., additional

Published
2022
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5. Tolerability, safety and survival in patients with severe pulmonary arterial hypertension treated with intravenous epoprostenol (Veletri®): a prospective, 6-months, open label, observational, non-interventional study.

Author

Degering, Julia, Egenlauf, Benjamin, Harutyunova, Satenik, Benjamin, Nicola, Salkić, Amina, Xanthouli, Panagiota, Eichstaedt, Christina A., Seeger, Rebekka, Sitbon, Olivier, and Grünig, Ekkehard

Subjects
PULMONARY arterial hypertension, PROSTACYCLIN, OVERALL survival, TERMINATION of treatment, PATIENT safety
Abstract

Background: Epoprostenol AS (Veletri®), a thermostable epoprostenol formulation, provides better drug stability and improved clinical use compared to previous epoprostenol formulations. This study aims to expand clinical experience in the use of Veletri®, especially regarding tolerability, safety and survival. Methods: Pulmonary arterial hypertension (PAH) patients at high risk despite pretreatment with at least double oral combination therapy and with clinical indication for epoprostenol (Veletri®) treatment were consecutively included in this prospective, open label, observational, non-interventional study. Clinical data were assessed at baseline, after 3 and 6 months. Adverse events (AEs) and serious adverse events (SAEs) were documented. Survival from initiation of Veletri® was assessed at last patient out. Results: Fifteen patients (60 ± 13.7 years, WHO functional class III (n = 10) or IV (n = 5), severely impaired right ventricular function, mean pulmonary arterial pressure 54.8 ± 8.9 mmHg, mean pulmonary vascular resistance 4.4 ± 0.7 (median 3.8) Wood Units) were enrolled and treated with a mean dosage of 7.9 ± 3.9 (median 7.5) ng/kg/min. Eleven patients completed the study (treatment withdrawal n = 1, death n = 3). After a mean follow-up of 19.1 ± 13.5 (median 18.0) months, seven patients died and three were listed for lung transplantation. Seven AEs (nausea n = 3, diarrhea n = 1, flushing n = 2, headaches n = 1) and three SAEs (catheter infection n = 2, catheter occlusion n = 1) were related to Veletri®. The 1- and 2-year survival rates were 73.3% and 52.4%, respectively. Conclusions: The study showed that safety and tolerability of epoprostenol AS (Veletri®) was comparable to previous prostacyclin formulations and was feasible for most patients. The maximum tolerable dosage was lower than dosages reported in the literature. In future applications/trials the up-titration process should be pushing for higher dosages of epoprostenol in the occurrence of side effects, as the achievement of a high and effective dosage is crucial for the clinical benefit of the patients. Survival was as expected in these prevalent severely impaired patients. Trial registration The study was registered in the EUPAS registry (EUPAS32492). [ABSTRACT FROM AUTHOR]

Published
2023
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